he parotid glands are small exocrine glands that rarely call attention to themselves.

Perfect
function throughout life is normal.
Dry mouth, drooling, swelling, and pain are essentially the only symptoms caused by
dysfunction of the salivary glands.
The major salivary glands and their ducts are strategically situated on either side of the dental
occlusal planes to irrigate and saturate a food bolus with saliva during chewing. The parotid
gland contacts the mandibular ramus and muscles of mastication, which massage the gland
during chewing. The mechanical squeezing and the parasympathetic nervous system, which
analyzes a number of sensory inputs, cause the glands to inject an appropriate quantity and
quality of saliva into the oral cavity. Minor salivary glands are scattered throughout the oral
cavity and pharynx to assist the major glands in moistening, lubricating, and protecting the
teeth and mucosa. The normal flow of saliva though the duct prevents oral bacteria from
ascending the duct to cause infection.
Inflammatory swelling of the glands may present a serious diagnostic challenge. Parotitis
presents in many forms and the symptoms vary from modest to prostrating. Reading the
numerous journal on parotitis articles reveals frequent contradictions in the classification,
etiology, and treatment of the disorders. A pure viral or bacterial infection, an autoimmune
inflammation, or a combination of these can be the etiology. In this article, evolution of the
knowledge of parotitis, as well as the diagnosis and treatment, is discussed.

Infectious parotitis
This group of diseases is caused by known infectious agents.

Acute bacterial parotitis

Acute bacterial parotitis is now infrequent, but its historical importance and occasional
occurrence today necessitate in-depth knowledge of this entity by the otolaryngologist.
Mumps and bacterial parotitis were differentiated by 1800, but neither was effectively
treated. The mortality rate for bacterial parotitis was 80%. Before antibiotics and intravenous
administration of fluids were available, bacterial parotitis occurred in postoperative patients
or other severely ill patients who became dehydrated and contributed to their demise as an
incurable sepsis.
Early in the 20th century, surgeons were hesitant to incise and drain parotid abscesses and
frequently used ineffective conservative measures until the process was irreversible. They
feared the consequences of the unsightly scar and facial paralysis. Parotid abscess is depicted
in the image below.

Elderly man with parotid abscess.

In 1917, Lilienthal described a surgical treatment that was very similar to what is used today.
[1]
He called parotid abscesses celiac parotitis because they were believed to be metastatic
from abdominal infections. Other authors used names such as acute surgical parotitis, acute
necrotic parotitis, acute gangrenous parotitis, and other historical designations according to
Hemenway and English in 1971.[2]
Lilienthal designed a vertical incision just anterior to the auricle that coursed posteriorly and
inferiorly below the ear to join and follow an upper cervical skin crease that paralleled the
lower mandibular border as seen in the image below.[1] He elevated the outlined skin flap
forward to expose the parotid gland and made multiple incisions into the gland parallel to the
facial nerve branches. He then opened the fascia behind the angle of the mandible to drain
deeper spaces. The wound was packed and healed by secondary intention, resulting in a
surprisingly good cosmetic result. The number of patients treated by this drainage is not
known, but this treatment was probably almost anecdotal to Lilienthals contemporaries.

Incision outlined for incision and drainage of

parotid abscess.
In 1919, Zachary Cope, a British Army surgeon, described 7 patients with parotitis that he
had treated in Baghdad during the exceptionally hot summer of 1917.[3] He recorded that these
soldiers had heatstroke or were severely affected by the extreme heat. The patients developed
parotid swelling accompanied by fever and general malaise. Cope made wide T-shaped
incisions in the gland to allow drainage. Four of the 7 survived after sloughing gangrenous
parotid tissue. Cope stated that although the disease was a bacterial infection, the excessive
heat and debilitating illness predisposed to its development.
In 1923, Blair and Padgett of St. Louis published an article stating that early surgical drainage
of the infected gland was safe and frequently was life saving.[4] They stated that acute
suppurative parotitis was an ascending duct infection related to decreased salivary flow, fever,
and general debilitation. They cultured the pus and found that Staphylococcus aureus was the
most common organism. The treatment proposed by Blair and Padgett did not become the
standard practice for several more years. However, the high mortality rate decreased early in
the 20th century and was 30-50% by 1930, probably because of more prompt and effective
drainage of the abscesses.
From the 1930s to the 1960s, irradiation treatment of numerous diseases became popular, and
several authors advocated 4-6 Gy delivered over 4-5 days for bacterial parotitis. Most patients
with severe infections required surgical drainage despite radiation treatment. By 1960, most
published papers stressed large doses of antibiotics, improved oral hygiene, and increased
fluid intake as treatment, with incision and drainage for failures. They found that the parotid
capsule and septations required wide exposure and extensive deep incisions parallel to the
facial nerve branches to exteriorize the diseased gland. Physicians recognized the importance
of hydration and oral hygiene for debilitated patients, and the incidence of bacterial parotitis
plummeted.

Parotitis is now more common in elderly patients because many take medications with an
atropine effect that retards salivary flow and predisposes to ascending infection. Many
psychotropic drugs are relatives of antihistamines.

Acute parotitis in neonates

This rare form of parotitis is lethal without treatment. In January 2004, Spiegel et al reviewed
the literature and stated that only 32 cases had been reported in journals during the previous 3
decades.[5] The characteristic clinical picture was of a sick premature infant with unilateral
parotid swelling and inflammation. Seventy-five percent of the cases were in male infants.
Pus expressed from the duct cultured S aureus in more than half of the cases. Most all of the
cultured bacteria were from organisms present in the oral cavity, which suggests an ascending
infection from the mouth.
Treatment is prompt administration of gentamicin and antistaphylococcal antibiotics plus
adequate hydration, with a cure in approximately 80% of cases. Failure to improve after 2448 hours of treatment necessitates surgical drainage. Recurrence is uncommon. Acute
bacterial parotitis in children between one year of age and adolescence is extremely rare and
only a few have been reported. The etiology and treatment is the same as for adults.

Chronic bacterial parotitis

Chronic bacterial parotitis may exist in the presence of calculi or stenosis of the ducts
secondary to injury. A number of articles and book chapters describe that chronic infection is
a sequela of acute bacterial infection, but the evidence is scant. Most authors have suggested
that decreased salivary flow was the common denominator, but reduced flow may be due to
the inflammation. In most instances, the chronic disease is either autoimmune or of unknown
etiology with superimposed bacterial infections and should not be designated as a chronic
bacterial infection.

Acute viral parotitis (mumps)

Mumps, one of the classic childhood infections, is spread by droplets or by direct spread from
oropharyngeal secretions that contain the paramyxovirus. Universal immunization, which
began in 1977, has made the clinical disease unusual in developed countries. The child should
receive the first measles, mumps and rubella (MMR) vaccine at age one year and a second at
age 4-6 years.[6, 7, 8]
Occasional outbreaks of mumps are seen, mostly in teenagers or patients in their early
twenties who did not receive the second shot. Before the vaccines were available, exposure
was almost universal, and clinical disease resulted in 60-70% of those who were exposed.
The disease was characterized by grossly enlarged and modestly tender parotid glands.
Parotid stimulation caused pain in the gland and ear. Mumps was a benign disease in the vast
majority of cases but was occasionally complicated by meningoencephalitis, pancreatitis,
orchitis, or deafness especially in young adults. Treatment was and is symptomatic and
supportive.